Lack of sweat (Hypohyrdrosis)

Well, I did find something on this subject, which makes me think that there is something to it…but not a lot. It’s not really that important…just an observation. I also notice a lot of tinitus these last couple of years, but maybe that is just another nasty side-effect of the aging process. Either that, or too much Led Zeppelin back in the 60’s!! Ha ha.

[B]Manifestations of Peripheral Autonomic Insufficiency in Patients Suffering from Acute Inflammatory Demyelinating Neuropathies [/B]

Abstract We tried to characterize the frequency and significance of manifestations of peripheral autonomic insufficiency (PAI) in clinical cases of [B]acute inflammatory demyelinating neuropathies (AIDN). [/B]Forty patients with the above diagnosis (21 men and 19 women, 16 to 72 years old) were examined. To detect symptoms attributable to PAI, we used Birkmayer–Vein tables; these data were compared with the results of electroneuromyographic (ENMG) examinations. In 38 and 2 cases, clinical manifestations of AIDN corresponded to the Guillain–Barre and Miller–Fisher syndromes, respectively. According to ENMG data, changes in the peripheral nerves and neuromuscular junctions corresponded to axonopathy, myelinopathy, and a mixed damage (myelinoaxonopathy) in 18 (45%), 14 (35%), and 8 (20%) patients, respectively. The following disturbances in the sphere of autonomic control were observed: orthostatic hypotension, in 28 cases (70%); tachycardia in the resting state, in 24 cases (60%); hypertension in the reclining position, in 16 cases (40%); [B]hypohydrosis of the skin on the limbs, in 18 cases (45%); [/B]dyspepsia, in 8 cases (20%), and enuresis, in 3 cases (7.5%). Manifestations of PAI began to be observed in the earliest stage of the disease and were preserved within the period of recovery of the motor functions; they were more intensive in the cases of a severe clinical course of polyneuropathies. The severity of autonomic disorders strictly correlated with the level of axonal degeneration (characterized according to the ENMG data). The treatment used (i.v. injections of immunoglobulin, plasmapheresis, use of vasoactive and neurometabolic drugs) not only improved the state of the motor sphere but also decreased the intensity of PAI symptoms. Thus, in the cases of AIDN not only thick myelinated fibers of the peripheral nerves but also a significant proportion of thin fibers responsible for the control of automatic functions are subjected to damage. PAI is rather frequently observed in patients suffering from AIDN, and the level of its manifestation reflects the severity of the disease and intensity of damage to the peripheral nerves.

Regards
Andrew